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A 29 year old female with systemic lupus erythematosus had a splenic infarct. The echogram showed a 4 x 4 x 5 cm cluster of echoes. After splenectomy the preoperative echograms were matched to the gross pathological findings and a post mortem water bath scan. In this single patient, the echosplenograms were of considerable aid in confirming the accuracy of the diagnosis of splenic infarct.
Gastric and splenic infarction following intraarterial infusion of vasopressin in a patient's left gastric artery is reported. None of the previously described factors predisposing to infarction were present and the cause appears to have been hyperconstriction of vessels in response to vasopressin. Computed tomography (CT) scanning was used to confirm the extent of involvement.
The association of sickle cell trait (SCT) and hereditary spherocytosis (HS) has been reported in only 18 patients. Three of these 18 patients experienced splenic infarct or acute splenic sequestration. We report here a 46-year-old African-American male, the oldest reported case to date, who experienced episodes of hemolysis and severe left upper quadrant pain for the past 26 years. The patient had compensated hemolysis with splenomegaly. A CT scan of the abdomen revealed a large infarct in the spleen. The diagnosis of SCT was confirmed with isoelectric focusing, cation exchange and reverse-phase HPLC. The presence of a silent, interacting globin variant as the cause of hemolysis and sickling in the spleen was ruled out by sequencing of the alpha1-, alpha2- and beta-globin genes. The diagnosis of HS was established by an osmotic fragility test. The interaction of HS and SCT leads to RBC dehydration with increased MCHC and intracellular Hb S concentration presumably favoring intrasplenic sickling and resultant splenic infarcts and sequestration as seen in this case.
The computed tomographic (CT) findings in eight patients with splenic infarction are described and correlated with ultrasound (US) in three. The diagnosis was proven in four by splenectomy or autopsy, in three by comparison with CT, having been obtained shortly before infarction, and in two by angiography. In four patients the infarct occurred as a result of hepatic or splenic artery embolization. The CT features of infarction may be difficult to differentiate from those due to trauma, inflammation or tumor, and include either a diffuse, a well circumscribed or an irregularly marginated area of low density within the spleen. Classical wedge-shaped defects are occasionally seen in the periphery of spleen. The ultrasonographic feature is usually that of a hypoechoic or an anechoic area in the spleen. In one patient, it became necessary to perform an ultrasound guided aspiration biopsy to rule out splenic abscess.
We present a case of splenic infarct during infectious mononucleosis in a 17-y-old boy. The patient's condition improved without the need for surgery.
A 74-year-old woman with secondary erythrocytosis was found to have Howell-Jolly bodies in peripheral blood erythrocytes following acute splenic infarction. The Howell-Jolly bodies were a transitory finding and disappeared six days after the infarction, although the spleen remained abnormal by isotope scanning for several weeks. Careful inspection of the peripheral blood film may be an aid in the diagnosis of acute splenic infarction.
The spleen in newborns, infants, and children is rarely involved in a variety of pathological processes. These processes may involve an isolated splenic disease or may be a part of a systemic illness. Renal vein thrombosis in infants of diabetic mothers has been reported. We report a case of a newborn with intestinal obstruction caused by an infarcted splenic hemangioma and renal vein thrombosis. To the best of our knowledge, this is the youngest case with both above-mentioned diagnoses and causes of intestinal obstruction in the English medical literature.
A 75-year-old man, previously diagnosed as having chronic myelomonocytic leukemia, suffered an attack of severe left hypochondralgia in July 1986. A splenic infarction was diagnosed by both ultrasound tomography and computerized tomography. The patient was treated with alpha-Interferon (600 M.U./day i.m.) for cytoreduction in order to prevent a recurrence of the splenic infarction. Twenty-one days later, the peripheral white blood cell count decreased from 44,110 microliters to 9800/microliters and the monocytoid immature cells disappeared. However, severe dementia appeared and so alpha-Interferon therapy was abandoned. In this report the beneficial effects and side effects of alpha-interferon in the treatment of chronic myelomonocytic leukemia are discussed.
Investigation of the role of vasoconstriction in the production of infarcts would be facilitated by a model based on a non-essential and readily accessible organ. Therefore, we investigated the effects of intraperitoneal injections of vasoconstrictor drugs on spleen and liver in the rat. Phenylephrine produced infarcts of the spleen regularly and infarcts of the liver occasionally. Epinephrine was also effective in rats that had been pretreated with tilorone. The lesions were caused by local (topical) effects of the drugs. In support of this conclusion, reduced perfusion of the target areas was demonstrated in vasoconstrictor-treated rats given India ink intravenously. In addition, splenic infarcts were produced either by intraperitoneal injection or by direct application of epinephrine to the surgically exposed spleen. On the contrary, splenic infarcts were not produced by injections of epinephrine outside the peritoneal cavity, or by intraperitoneal injections if the spleen had been transposed outside of the cavity beforehand. Thus, we have produced an experimental model of splenic infarcts caused by topical application of vasoconstrictor drugs which is reminiscent of the speckled spleen (Fleckmilz) of human pathology.
Invasive aspergillosis is a rare but important cause of morbidity and mortality in patients with AIDS. In the majority of patients, invasive aspergillosis involves the lungs. Extrapulmonary involvement with total splenic infarction has not been previously described. We illustrate a patient who developed total splenic infarction and septic emboli to the brain from Aspergillus.
Invasive aspergillosis is a rare but important cause of morbidity and mortality in patients with AIDS. In the majority of patients, invasive aspergillosis involves the lungs. Extrapulmonary involvement with total splenic infarction has not been previously described. We illustrate a patient who developed total splenic infarction and septic emboli to the brain from Aspergillus.
Acute respiratory distress syndrome (ARDS) is the most severe lung injury caused by many pathologic states. We treated a patient who suffered from ARDS caused by splenic infarction. A 75-year-old patient had a gastric cancer with multiple lung and liver metastasis. During anti-cancer therapy, she developed a high fever (above 39 degrees C) and a chest and an abdominal CT scan revealed splenic infarction. Hypoxia progressed gradually and she was transferred to ICU with tracheal intubation. Mechanical ventilation was performed according to open lung strategy, but she did not recover. On ICU day 3, the bilateral infiltration shadow on her chest X-ray was pointed out, and she had a low central venous pressure. We diagnosed her ARDS. The administration of methylprednisolone was started according to Meduri's report. Hypoxia was improved gradually and on ICU day 7, she was weaned from mechanical ventilation, and extubated. On ICU day 8, she was returned to her ward without ventilatory support.
The authors report a scintigraph of a 76-year-old man interpreted as being of a partially herniated spleen constricted by the diaphragm. The constriction proved illusory.
Two patients with end-stage renal disease from diabetes mellitus on peritoneal dialysis for 2 or more years developed sterile peritonitis secondary to splenic infarcts with associated peripheral embolic phenomena. The dialysate had WBC counts > 200/microL, of which 70% or more were polymorphonuclear cells, and RBC counts of 60/microL or less, although transient hemoperitoneum occurred in both patients. Extensive atherosclerotic vascular disease as well as hematologic abnormalities were also present in both patients. One patient had polycythemia due to decreased plasma volume. The other patient had evidence of dysfibrinogenemia. The patients responded well to anticoagulation with warfarin. When the warfarin was discontinued, recurrent emboli occurred in both patients. Splenic infarct should be included in the differential diagnosis of diabetic patients with atherosclerotic disease who present with sterile peritonitis that does not respond to antibiotic therapy, especially if hemoperitoneum occurs even transiently. The diagnosis can be confirmed with CT scan of the abdomen. Warfarin therapy is effective in preventing recurrent embolic phenomena, but may need to be continued indefinitely.
Patients with extensive atherosclerosis are at increased risk of developing embolic complications during cardiac catheterization. We describe a 51-year-old man with unstable angina and bilateral leg claudication who developed fever and right upper abdominal pain shortly after cardiac catheterization. Liver-spleen scintigraphy demonstrated a wedge-shaped filling defect compatible with splenic infarction, and serial scans performed over a period of five months showed resolution of this finding. Splenic infarction tends to be under-diagnosed, and physicians should be aware of this potentially serious complication of cardiac catheterization.
Although patients with AIDS frequently develop high titers of anticardiolipin antibodies, the clinical significance of this laboratory abnormality in AIDS patients is unknown. A 33-year-old female with AIDS, a prior small cerebrovascular accident, thrombocytopenia, and a coagulopathy suddenly developed left upper quadrant pain and tenderness due to splenic infarction associated with a high titer of anticardiolipin antibodies. Possible clinical manifestations of anticardiolipin antibodies in this patient include recurrent thromboembolism, coagulopathy, and thrombocytopenia. This case report suggests that anticardiolipin antibodies are associated with splenic infarction and that anticardiolipin antibodies associated with AIDS may sometimes be clinically significant.
A 54-year-old woman had been treated for hypertrophic cardiomyopathy and paroxysmal atrial fibrillation since 1992. She was admitted with paroxysmal atrial fibrillation which was resolved by medical treatment. However, on the next day, left lateral chest pain appeared. Computed tomography disclosed a low density area in the spleen. She received anticoagulant therapy under a diagnosis of splenic infarction, and the pain disappeared. Echocardiography showed hypertrophic cardiomyopathy with mid-ventricular obstruction. She was treated with cibenzoline to prevent paroxysmal atrial fibrillation attack and attenuate the hemodynamic load. After treatment, the pressure gradient decreased from 41 to 7 mmHg. This patient with hypertrophic cardiomyopathy suffered a rare isolated splenic infarction associated with paroxysmal atrial fibrillation.
BACKGROUND: Aneurysms of visceral arteries are rare, but may lead to dramatic situations of intraabdominal or retroperitoneal hemorrhage in case of rupture. CASE REPORT: We report the case of a 72-year-old patient who developed a hemorrhagic shock following a total hip replacement due to the rupture of an aneurysm of the gastroduodenal artery. Angiography also demonstrated a high-grade stenosis of the celiac trunk. The ruptured aneurysm was ligated as a live-saving procedure, but due to the stenosis in the celiac trunk the patient developed a splenic infarction followed by partial tissue liquefication. This was treated conservatively and after 3 months, the computed tomography showed an atrophic residual spleen. SUMMARY: Diagnostic and therapeutic approaches to visceral vascular aneurysms are discussed including the potential complications of splenic infarction.